Endocrine
Thyroid disorders encompass underactive thyroid (hypothyroidism), overactive thyroid (hyperthyroidism/thyrotoxicosis), structural changes (goiter, nodules), and autoimmune conditions (Hashimoto’s thyroiditis, Graves’ disease). Western medicine defines and monitors thyroid status biochemically—principally using TSH, free T4, and when indicated, total/free T3 and thyroid antibodies (anti-TPO, anti-thyroglobulin, and TSH receptor antibodies [TRAb]). Imaging (ultrasound) and functional tests (radioactive iodine uptake [RAIU]) help characterize nodules and distinguish causes of thyrotoxicosis. Treatment decisions weigh severity, etiology, symptoms, pregnancy status, age, and comorbid risk (cardiovascular, bone).
Hypothyroidism is most often autoimmune (Hashimoto’s) in iodine-sufficient regions. The gold standard treatment is levothyroxine (synthetic T4), titrated to normalize TSH and alleviate symptoms, with rechecks 6–8 weeks after dose changes and at steady state. Debate persists about adding liothyronine (T3) for persistent symptoms despite normalized TSH; current guidelines reserve combination therapy for carefully selected, monitored trials after ruling out other causes. Subclinical hypothyroidism (elevated TSH, normal FT4) management is individualized: treatment is favored when TSH ≥10 mIU/L, in pregnancy or infertility, with significant symptoms, goiter, positive TPO antibodies, or in younger patients planning conception; watchful waiting is often reasonable otherwise. Special attention to drug and nutrient interactions (iron, calcium, proton pump inhibitors, soy, high-fiber diets) and conditions that impair absorption (celiac disease, H. pylori, atrophic gastritis) is essential.
Hyperthyroidism most commonly arises from Graves’ disease, toxic multinodular goiter, or a toxic adenoma. First-line options include antithyroid drugs (methimazole; propylthiouracil [PTU] in the first trimester of pregnancy or for thyroid storm), radioactive iodine ablation, and thyroid
Well-Studied